Abstract Intracerebral Hemorrhage is a subtype of hemorrhagic stroke that has devastating consequences when it occurs in humans. Broadly there are two mechanisms of neuronal damage that occurs in the event of an ICH. The early brain injury is secondary to the hematoma itself and early erythrolysis within 24 hours of the injury. Delayed brain injury is mediated by various pathways related to the scavenging of the hematoma by the macrophage system. There is reasonable animal model data that validates pathomechanisms of delayed neurotoxicity following an ICH. Ultra-early erythrolysis is a novel phenomenon that has been observed in a recent animal ICH model study by the authors. In this rat model there is good correlation of early erythrolysis with hypo or isointensity on T2* sequences within the hematoma within first 24 hours after an ICH and increased tissue iron levels in the perihematomal brain tissue on histology. There is no such correlative phenomenon that has been documented in the human population. The proposed study will attempt to confirm or refute the presence of the phenomenon of ultra-early erythrolysis and mediated neuronal injury due to increased iron levels in the periphery of the hematoma based on MRI. Various MRI parameters like volume of T2* iso/non-hypointensity within the hematoma, R2* value in the periphery of the hematoma and volume of edema on FLAIR sequence will be measured on day 1, day14 and day 30 to evaluate the presence of the phenomenon of ultra-early erythrolysis in ICH in human subjects, not only in the first 24 hrs but also up to 30 days following the hematoma.